In recent years, attention has been focused on activated autologous lymphocyte therapy, which comprises taking immunocompetent cells (lymphocytes in particular) in blood out of the body, culturing them for stimulation/activation and for proliferation and again returning them into the body to thereby prevent the advance of cancer. This technique produces little side effects and makes it possible to maintain the quality of life (QOL) at high levels even during treatment and, therefore, is becoming more and more popular in the field of cancer treatment as a fourth choice of cancer therapy next to the three major cancer treatment methods, namely surgical therapy, radiotherapy and chemotherapy. The technique is already in actual use as one of tailor-made highly advanced medical treatment methods in university hospitals, cancer centers and specialized clinics and, expectedly, it will be used still more widely. This technique generally comprises collecting a portion of the blood of a patient, separating a lymphocyte fraction by density gradient centrifugation, adding the autologous plasma to a medium for exclusive use and cultivating the lymphocytes. Generally, the number of lymphocytes arrives at about 100 times the number of lymphocytes in the primary culture in a week. It has become known, however, that there are some such cancer patients that lymphocytes derived therefrom can hardly proliferate in the presence of autologous plasma but can proliferate in the presence of the plasma derived from another person (resulting from blood donation). Cancer cells produce cellular immunity inhibiting factors, for example such cytokines as transforming growth factor beta (hereinafter abbreviated as TGF-β), interleukin 4 (hereinafter abbreviated as IL4), interleukin 6 (hereinafter abbreviated as IL6) and interleukin 10 (hereinafter abbreviated as IL10) as well as prostaglandin E2 (hereinafter abbreviated as PGE2). Thus, the possibility is suggested that such factors might inhibit the proliferation of lymphocytes. However, the concentrations of these factors in the blood of cancer patients are almost the same as those in persons in normal health, although their local concentrations in cancer foci are high. Further, when such factors commercially available as reagents are dissolved in plasma at high concentrations and the influences thereof on lymphocyte proliferation are examined, little inhibition is observed. Such and other findings suggest that there is an unknown mechanism other than the involvement of such factors.
As a matter of fact, an adsorbent for adsorptively removing immunosuppressive acidic proteins (IAPs) (Patent Document 1), an adsorbent for adsorptively removing interleukins in body fluids (Patent Document 2) and an adsorbent capable of adsorbing TGF-β in body fluids (Patent Document 3), among others, have so far been disclosed. However, all of them are limited in scope to the adsorptive removal of cytokines and there is no report about an adsorbent capable of improving the proliferative activity of lymphocytes. In recent years, the number of patients having activated lymphocyte therapy has been increasing year by year with the marked advance of such therapy and, on the other hand, the number of patients relying on blood donation because of poor lymphocyte proliferation has also been increasing. In the case of blood donation, it is necessary to secure non-autologous plasma in conformity with patient's therapeutic cycle. Further, there are a number of problems to be taken up from the safety viewpoint, for example the risk of infection; therefore, it is desired that a method for overcoming the lymphocyte proliferation inhibition in lymphocyte culture by a simple procedure without losing other useful substances be developed. Furthermore, in cancer patients as well whose lymphocyte can proliferate in the presence of autologous body fluids, it is expected that further improvements in proliferation rate and in cytokine producing activity, for instance, be achieved when the inhibition of lymphocyte proliferation in lymphocyte culture is broken down. Currently, however, neither adsorbent, nor porous body, nor device nor treatment method is available for such purposes. Further, adsorbents prepared by causing a material capable of adsorbing cytokines and like immunosuppressive proteins to bind to a water-insoluble carrier have been disclosed (Patent Document 4 to 6). However, the effect of those adsorbents depends on an affinity between an amine residue and such immunosuppressive proteins as cytokines. Therefore, those adsorbents require the presence of an amine residue.
At present, a treatment is eagerly anticipated which will promote the proliferation of those lymphocytes which are in a poorly proliferative condition in lymphocyte culture for the treatment of a disease against which a therapy comprising returning activated lymphocytes again into the body, typically activated autologous lymphocyte therapy, is therapeutically effective.    Patent Document 1: Japanese Kokai Publication Sho-56-092824    Patent Document 2: Japanese Kokai Publication Hei-08-257398    Patent Document 3: Japanese Kokai Publication 2001-218840    Patent Document 4: Japanese Kokai Publication 2003-310751    Patent Document 5: Japanese Kokai Publication 2003-339854    Patent Document 6: Japanese Kokai Publication 2004-73618